Murray-Zmijewski F, Lane D P, Bourdon J-C
Department of Surgery and Molecular Oncology, University of Dundee, Ninewells Hospital, CR-UK Cell Transformation Research Group, Dundee DD19SY, UK.
Cell Death Differ. 2006 Jun;13(6):962-72. doi: 10.1038/sj.cdd.4401914.
p63, p73 and p53 compose a family of transcription factors involved in cell response to stress and development. p53 is the most frequently mutated gene in cancer (50%) and loss of p53 activity is considered to be ubiquitous to all cancers. Recent publications may have a profound impact on our understanding of p53 tumour suppressor activity. p63, p73 and p53 genes have a dual gene structure conserved in drosophila, zebrafish and man. They encode for multiple p63, p73 or p53 proteins containing different protein domains (isoforms) due to multiple splicing, alternative promoter and alternative initiation of translation. In this review, we describe the different isoforms of p63, p73, p53 and their roles in development and cancer. The changes in the interactions between p53, p63 and p73 isoforms are likely to be fundamental to our understanding in the transition between normal cell cycling and the onset of tumour formation.
p63、p73和p53构成了一个转录因子家族，参与细胞对应激和发育的反应。p53是癌症中最常发生突变的基因（50%），p53活性的丧失被认为在所有癌症中普遍存在。最近的出版物可能会对我们对p53肿瘤抑制活性的理解产生深远影响。p63、p73和p53基因具有在果蝇、斑马鱼和人类中保守的双基因结构。由于多种剪接、可变启动子和可变翻译起始，它们编码包含不同蛋白质结构域（异构体）的多种p63、p73或p53蛋白。在这篇综述中，我们描述了p63、p73、p53的不同异构体及其在发育和癌症中的作用。p53、p63和p73异构体之间相互作用的变化可能是我们理解正常细胞周期与肿瘤形成起始之间转变的基础。
